| 1. | Permanent middle cerebral artery occlusion , pmcao
方法采用大鼠永久性大脑中动脉阻塞 |
| 2. | Middle cerebral artery occlusion , mcao
大脑中动脉闭塞 |
| 3. | Experiment about single - strand dna breaks in permanent middle cerebral artery occlusion of rats
单链断裂损伤的实验研究 |
| 4. | Time course of regional cerebral blood flow in middle cerebral artery occlusion model in rats
大鼠大脑中动脉局灶性脑缺血局部脑血流动态观察 |
| 5. | Establishment and evaluation of the model of middle cerebral artery occlusion reperfusion in mice
小鼠大脑中动脉闭塞再灌注模型的建立和评价 |
| 6. | Comparative proteomic analysis of cerebral cortex between middle cerebral artery occlusion rats and normal controls
正常与脑缺血大鼠的脑皮质蛋白质差异分析鉴定 |
| 7. | Effect of electroacupuncture on bdnf expression at ischemia cortex and infarct volume after middle cerebral artery occlusion in rat
累加电针对脑缺血大鼠皮层脑源性神经营养因子表达及脑梗塞体积的影响 |
| 8. | The present study determined if the potent and nonaromatizable androgen , dihydrotestosterone ( dht ) , exacerbates ischemic damage in the male rat and alters postischemic gene expression after middle cerebral artery occlusion
新近研究对有效的未芳香化的雄激素，双氢睾酮，是否会加剧雄性大鼠的缺血损伤并改变大脑中动脉闭塞后的缺血后基因表达进行了研究。 |
| 9. | To make clear the hypothesis , a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study , respectively . we first studied the cellular localization of kvl . 2 and the co - localization of kvl . 2 protein and vegf receptors flk - 1 and flt - 1 , observed the effect of mcao on kvl . 2 expression and phosphrylation in the rat brain in vivo , then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl . 2 in sh - sy5y cells . finally , in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl . 2 phosphorylation , we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl . 2 phosphorylation
为了验证上述假设，本文分别在整体和离体水平，采用大脑中动脉缺血( middlecerebralarteryocclusion ， mcao )和体外氧?糖剥夺( hypoxiaandglucose - deprivation ， hgd )缺血模型，首先了解了kv1 . 2蛋白的细胞定位及与vegf受体flk - 1和flt - 1的共存情况，观察了整体mcao后缺血再灌不同时间大鼠脑内kv1 . 2蛋白的磷酸化水平变化，然后通过外源性给予vegf蛋白，在sh - sy5y细胞株上观察其对缺血细胞存活率及kv1 . 2蛋白磷酸化水平的影响，最后利用vegf反义脱氧寡核苷酸( oligodeoxynucleotide ， odn )特异阻断内源性vegf蛋白的表达，观察内源性vegf蛋白在缺血细胞损伤及调节kv1 . 2蛋白磷酸化中的作用，以进一步明确vegf缺血保护效应与其调节kv1 . 2蛋白磷酸化之间的关系。 |
